AMS Problems of the Heart

Heart Failure

• Clinical syndrome

• Structural and/or functional cardiac disorder (usually following an MI)

• Acute (exacerbations) and chronic presentations

• Long uncontrolled HTN

• CAD

• Diabetes, obesity

• Previous MI

• Sleep apnea

• Pulmonary issues (ex. smoking)

• Chemo

What are the some of the risk factors of HF?

• Inadequate cardiac output (CO)

• Compromised tissue perfusion

• Hypertrophy of the myocardium (HF with PRESERVED EF)

• Pulmonary and/or systemic congestion (HF with REDUCED EF)

What are the complications HF can result in?

• SOB

• Changes in mental

• Edema

What does decreased tissue perfusion manifest as?

Because the body is not adequately perfusing to the kidneys

Why would inadequate cardiac output result in low urine output?

Ejection Fraction (EF)

The amount of blood ejected from the heart during systole (contraction)

• Measures mainly percentage that goes out, but does not determine HF only diagnose

Systole

Heart contracts

Diastole

Heart relaxes and fills with blood

55-70%

What is the normal range of EF?

When <40%

When should you worry about the EF?

1. Transthoracic Echocardiogram (TTE)

2. Transesophageal Echocardiogram (TEE)

What are the two diagnostics for EF?

Transthoracic Echocardiogram (TTE)

• Non-invasive

• No special prep required (No NPO, no consent)

• Performed bedside or cardiology department (completed outpatient)

• DOES NOT view posterior and deeper structures as well

Transesophageal Echocardiogram (TEE)

• Invasive (scope into esophagus)

• Moderate sedation with CONSENT

• NPO 4-6 hours before; until gag reflex returns

• VIEWS posterior angle of heart

• Visualizes vegetation on valves and blood clots

• Posterior angle of the heart

• Vegetation on valves and blood clots

What does the TEE view that the TTE doesn’t view as well?

1. Left sided

2. Right sided

What are the two types of HF?

1. Systolic Dysfunction (HFrEF)

2. Diastolic Dysfunction (HFpEF)

What are the two subtypes of HF?

Right sided HF

• Right heart (ventricle) is unable to pump the volume of blood into lungs

• Increased right sided pressure

• Usually SECONDARY to chronic cardiac or pulmonary problems OR left sided HF

• Cor Pulmonale

Left sided HF

• Most common

• Reduced EF (<40% or Preserved 55-70%)

• Left ventricle is unable to pump with enough force to eject blood during systole

• Low CO from left ventricle

• Low tissue perfusion

• Increased pressure in pulmonary vessels (congestion, backs up into the lungs)

What happens in the heart and body during left sided HF?

Preload

Volume of blood in ventricles at end of diastole (end diastolic pressure)

Wears out heart muscles

What happens if a person has preload issues long term?

Afterload

Resistance left ventricle must overcome to circulate blood

Decreased contraction of the heart due to increased HTN and Vasoconstriction over a long period of time (more blood trying to get out against resistance)

What happens if a person has afterload issues long term?

• Pulmonary congestion

  • cough

  • crackles, wheezes

  • blood-tinged sputum

  • tachypnea

  • decreased breathing laying down

• Tachycardia

• Cyanosis (low perfusion)

• Fatigue

What are the s/s of left sided HF?

• Sympathetic nervous system stimulation

• RAAS activation

• Myocardial hypertrophy

• “Other” vasoconstriction:

  • Vassopression from posterior pituitary

  • Endothelin

What are the compensatory mechanisms in the body?

O2 in myocardium

What do all compensatory mechanisms increase demand for?

Development of s/s

What happens when demand for O2 is > myocardial reserve?

It increases workload of heart which can lead to HF

Why are compensatory mechanisms bad long term?

HR x SV

What is the equation for CO

• RAAS senses decreased CO, where kidneys aren’t getting perfused

• The decreased BP, makes RAAS release Renin which stimulate body to create AGT II

• AGT II is a vasoconstrictor which long term can lead to CARDIAC REMODELLING

• Preload and afterload also increase

• Body holds onto fluid

Why does the activation RAAS system long term lead to HF?

Cardiac Remodelling

Changes in the structrue and function of heart, which leads to heart developing scar tissue

Myocardial Hypertrophy

Enlargement of the myocardia, muscles thicken

• Heart is pumping really hard

• Heart begins to use collateral vessels during vasoconstriction

• Vessels are weak and can’t take a lot of pressure

(diastolic)

Why is myocardial hypertrophy bad long term?

Low perfusion to the brain which stimulates the release of ADH and increases water and Na retention (can contribute to HF)

Why does vasopressin get released during compensatory mechanisms when BP is low?

Endothelin

Vasoconstrictor, epithelial cells in blood vessel

Systolic Dysfunction (HFrEF)

• Most common form

• REDUCED EF (<40%)

• Poor CONTRACTILITY (PUMPING function) on echocardiogram

• Weakened heart muscle (thin) can’t squeeze as well

• Creates increased blood in heart

• Less blood is pumped out of ventricles (low EF)

What happens during systolic HF?

• Inadequate tissue perfusion (blood can’t get out)

• Pulmonary congestion (backing up)

• Systemic congestion

What are the manifestations of systolic HF?

Systolic (HFrEF)

• The lower the EF, the higher the risk

Which type of left sided HF creates a significantly increased risk for SUDDEN cardiac death?

Devices that help the heart pump: Cardiac defibrillator

• External: LifeVest

• Internal: ICD

What are some interventions for those with systolic HF in the hx?

Diastolic Dysfunction (HFpHF)

• PRESERVED EF (40% or higher)

• Ventricle is stiff and non-compliant

• Poor FILLING on echocardiogram

• Stiff (thickened) heart muscle can’t relax normally

• Creates less space for blood to fill ventricles

• High contractility (EF) bc of thicker muscles

What happens during diastolic HF?

Systemic vascular congestion and Peripheral edema

• Viscera and peripheral congestion (

• JVD

• Dependent edema

• Hepatomegaly (and spleen)

• Ascites

• Weight gain

• Decreased UOP while awake

• Nocturia

• Nausea, anorexia (feel full)

What are the manifestations of right sided HF?

• Patient is upright and the fluids tends to collect at the lower extremities instead of going to the kidneys

• Kidneys aren’t perfusing the fluids

• Increased UOP when patient is laying down

Why does right sided HF cause decreased UOP while awake?

• Left ventricular failure (Left sided HF)

• Right ventricular myocardial infarction

• Pulmonary hypertension

What are the causes of right sided HF?

• Echocardiogram: Assessment of LV function (EF) (ex. TTE, TEE)

• Electrocardiogram (ECG/EKG)

• Chest x-ray

• Stress test

• Cardiac cath

• Labs

What are the ways to diagnose HF?

• BNP

• Electrolytes

• Renal function

• Liver function (LFTs)

• CBC

• ABGs

What are the labs for diagnosing HF?

Brain Natriuretic Peptide (BNP)

• Hormone released by heart when working harder or under stress

  • HF, HTN, MI, Kidney disease (fluid retention)

• Stimulates vasodilation and diuresis (release water and Na)

BNP (negative in dyspneic individuals with lung disease)

What is used to determine if dyspnea is a result of HF or lung disease?

<100 pg/mL

What are the values of BNP if there is NO HF?

>900 pg/mL

What are the values of BNP when there is SEVERE HF?

• Improve cardiac function

• Reduce s/s

• Stabilize CO

• Delay progression of disease

• Enhance lifestyle changes

• Reduce Hx

• Increase survival

What are the goals of treatment in HF?

• Patient education (self mon s/s, med adhere, weigh)

• Lung assessment

• Med management

• Labs (follow up)

• VS (O2 sat)

• Cardiac monitoring

• I/O

• Daily weight

• Advance directives

What are the nursing interventions for HF?

• Med management

• Diet:

  • low sodium

  • fluid restriction

• Monitoring:

  • changes in fluid balance (edema)

  • Daily weights

  • Symptoms of disease progression

  • BP, HR

• When to call HCP

What is the patient education for HF?

• Digoxin

Cardiac remodelling

• ACE/ARBS

• Beta blockers

• Neprilysin Inhibitors: sacubitril/valsartan (Entresto)

What are the meds for HF?

Digoxin

• Cardiac glycoside med (Na/K pump)

• Positive Inotrope and Negative Chronotrope

• Used for SYMPTOMATIC, chronic HF patients with sinus rhythm or afib

  • decrease dyspnea, increase functional activity

• Absorbtion: GI tract

• Excretion: Kidneys

Where is digoxin absorbed and excreated?

Toxicity

What is the main risk for patients taking dignoxin?

If <60 BPM, call HCP

When do you hold digoxin?

Positive inotrope

Helps contractilty

Negative chronotrope

Slows HR (allows time for filling)

True (T)

T or F:

Cardiac remodelling can be reversed

Neprilysin Inhibitors: sacubitril/valsartan (Entresto)

• Stops neprilysin (stops breakdown of BNP and allows it to work longer); high BNP is expected

• Can cause fetal toxicity

• Heart transplantation

• Cardiac remodeling surgery

• Ventricular assist devices

• Automatic implantable cardiac defibrillator (AICD)

What are the interventions for advanced HF?

• Surgical ventricular restoration

• Left ventricular reconstruction (remove scar tissue)

Types of cardiac remodeling surgery?

• LVAD/RVAD

• Bridge until transplantation (or end of life)

Types of ventricular assist devices?

1. Endocarditis

2. Pericarditis

What are the types of tissue layer disorders in the heart?

Endocarditis

Inflammation of the endocardium caused by INFECTION (virus, fungus, bacteria)

• Age

• Congenital factors

• Prosthetic valve replacements

• IV drug use (directly into bloodstream)

• Bacteremia

• Poor dental hygiene/dental procedures (into gums)

• Rheumatic heart disease (permanent, heart valve damage)

What are the risk factors for endocarditis?

1. Normal endothelium that is typically resistant to pathogen

2. Bacterial adhesion to endothelium

3. Inflammatory response from body (WBC, platelets)

4. Thrombogenesis stops bacteria from flowing through and gets stuck in one place

5. Vegetation formation in that area

6. Vegetation can break off and travel somewhere else in body

What is the patho of endocarditis?

• Fever, chills, night sweats

• Fatigue

• Anemia

• Anorexia/weight loss

• Murmur (valular changes)

• HF (left or right)

• Petechiae, splinter hemorrhages

• Janeway lesions (palms, soles of feet)

• Osler’s nodes (tips of fingers, toes)

• Roth spots (retinal hemorrages)

What are the s/s of endocarditis?

• Pieces of vegatative plaque break off (emboli) and cause clots in other parts of the body

• Can lead to infarct in larger organs and increase other complications

• High mortality

Why do hemorrhages happen in other parts of the body during endocarditis?

• Blood Cultures (main)

• TEE (main)

• CBC

• CRP (inflammation)

• Chest x-ray

• Cardiac cath

5 c’s + T

What are the diagnostics for endocarditis?

• IV AB (long term)

• Monitor for signs of HF

• Rest

• Analgesics

• Aseptic techniques

• Surgical valve repair for replacement

• Prevent relapse

• Gently brush teeth, no flossing

What are the treatments for endocarditis?

• Assess: cardiac, fluids balance, embolic events

• Administer meds

• Support cardiac function

• Infection control (aseptic)

• Prevent complications (HF, PE, CVA)

  • SCDs, ambulate, labs

• Post op care

• Pt. edu on disease process

• Adhereance to tx plan: education

What are the nursing interventions for endocarditis?

Pericarditis

Inflammation of the pericardium (membranous sac that encloses the heart)

• Infective organisms (usually respiratory)

• Post-myocardial infarction (Dressler’s Syndrome)

• Post-pericardiotomy syndrome (also Dressler’s, but caused by chest trauma or surgery)

• Tuberculosis

• Radiation therapy

• Trauma

• Renal failure

• Metastatic cancer/malignancy

What are the risk factors of pericarditis?

Dressler’s syndrome

After there is injury to the heart, the body’s immune system is falsely triggered to reactivate its inflammatory response in pericardium

• Pain

  • similar to caridac ischemia (sub sternal or mid stermal radiates neck, shoulder, back)

  • Aggravated by inspiration

• Global ST elevation on 12-lead EKG

• Dyspnea

• Pericardial friction rub (inflammed layers rub together)

• Fever

• Increased WBC

• s/s HF

• Afib

What are the s/s pericarditis?

Sitting up and leaning foward

How do you relieve pain on inspiration in pericarditis?

• Echocardiogram (look for thickening)

• EKG (PR segment depression, ST elevation)

• Cardiac enzymes

• Chest x-ray (fluids)

What are the diagnostics for pericarditis?

• Treat underlying cause

• Control pain

• Positioning

• NSAIDS 24-48 hrs

• Steroids

• Antibiotics

• Periocardiocentesis

• Pericardial window

• Radiation/chemo (is cancer underlying)

What are the treatments for pericarditis?

Pericardiocentesis

Needle into the pericardium to drain fluid

Pericardial window

Surgical procedure to drain excess fluid into pleural space, then using chest tube for continued removal

Anti-inflammatory meds

What meds should you give if chemo is the is causing pericarditis?

• Bed rest

• Oxygen

• Pain relief

• Administer antibiotics

• Pt. and family education

• Assess for development of complicaions

What are the nursing interventions for pericarditis?

• Pericardial effusion

• Cardiac tamponade

What are the complications of pericarditis?

Cardiac tamponade

A rapid build-up of blood or other fluid (20-50mL) in pericardial sac that puts pressure on the heart, which prevents it from pumping effectively

• Heart goes into shock because it can’t compensate that quickly

• LIFE THREATENING WITHOUT TX

• Beck’s Triad

  • Hypotension (decreased CO) (heart can’t pump)

  • JVD

  • Muffled heart sounds (fluid around)

• Tachycardia (compensate)

• Paradoxical pulse (pulsus paradoxus)

What are the s/s cardiac tamponade?

Paradoxical pulse (pulsus paradoxus)

Inspiration causes more pressure to be placed on the heart and leads to decreased CO and BP

• Increased CO on exhalation

• Pericardiocentesis

• Pericardial window

• Pericardiectomy (remove pericardium in recurrent patients)

What are the interventons for cardiac tamponade?

Cardiomyopathy

Chronic disease of the heart muscle associated with ventricular dysfunction

• High mortality

1. Dilated cardiomyopathy (common)

2. Hypertrophic cardiomyopathy

3. Restrictive cardiomyopathy (rare)

4. Arrhythmogenic right ventricular cardiomyopathy

What are the 4 categories of cardiomyopathy?

Dilated cardiomyopathy

• Dilation of 1 or both ventricules (enlarged and weak)

• SYSTOLIC dysfunction (pumping) (NOT systolic HF)

• Results in decreased CO

s/s HF but not HF

• Dyspnea on exertion

• Decreased exercise capacity

• Palpitations

• Fatigue

What are the s/s dilated cardiomyopathy?

• Alcohol abuse

• Chemo

• Infection

• Inflammation

• Poor nutrition

What are the causes of dilated cardiomyopathy?

Hypertrophic cardiomyopathy

Thickening of left ventricle and intraventricular septum

• DIASTOLIC dysfunction

• Decreased CO

• Left ventricular outflow obstruction

Genetic component (about 50%)

What are the causes of hypertrophic cardiomyopathy?

Hypertrophic cardiomyopathy

Which heart condition causes sudden cardiac death in athletes?

• Depends on type

• Tx is like HF:

  • Diuretics

  • Vasodilators

  • Meds increasing contractility

  • Meds addressing compensatory responses

• Surgical

  • Transplant

  • Ventricular assistive device

  • AICD

What is the treatment for cardiomyopathy?